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hESC-derived Olig2+ progenitors generate a subtype of astroglia with protective effects against ischaemic brain injury. | LitMetric

AI Article Synopsis

  • Human pluripotent stem cells can be differentiated into various types of astroglia, but their effectiveness for treating neurological diseases has not been thoroughly researched.
  • A specific subtype of astroglia, called Olig2PC-Astros, is derived from Olig2(+) progenitors and shows significant differences in neuroprotective properties compared to traditional astroglia sourced from Olig2-negative progenitors.
  • When transplanted into brains affected by global ischaemia, Olig2PC-Astros demonstrate better neuroprotective effects and lead to improved behavioral outcomes, indicating their potential as a new cell therapy approach for neurological disorders.

Article Abstract

Human pluripotent stem cells (hPSCs) have been differentiated to astroglia, but the utilization of hPSC-derived astroglia as cell therapy for neurological diseases has not been well studied. Astroglia are heterogeneous, and not all astroglia are equivalent in promoting neural repair. A prerequisite for cell therapy is to derive defined cell populations with superior therapeutic effects. Here we use an Olig2-GFP human embryonic stem cell (hESC) reporter to demonstrate that hESC-derived Olig2(+) progenitors generate a subtype of previously uncharacterized astroglia (Olig2PC-Astros). These Olig2PC-Astros differ substantially from astroglia differentiated from Olig2-negative hESC-derived neural progenitor cells (NPC-Astros), particularly in their neuroprotective properties. When grafted into brains subjected to global ischaemia, Olig2PC-Astros exhibit superior neuroprotective effects and improved behavioural outcome compared to NPC-Astros. Thus, this new paradigm of human astroglial differentiation is useful for studying the heterogeneity of human astroglia, and the unique Olig2PC-Astros may constitute a new cell therapy for treating cerebral ischaemia and other neurological diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3903179PMC
http://dx.doi.org/10.1038/ncomms3196DOI Listing

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